IntRoductIonBone is considered to be one of the hardest living tissues which has an extensive blood supply and is constantly undergoing change [1]. Osteoblasts account for the organic components of bone matrix. Bone surface growth is promoted by deposition of calcium salts in a newly formed matrix [2]. Alkaline phosphatase secreting Osteoblasts, generate matrix vesicles in which crystals of hydroxyapatite (calcium and phosphate deposits) are shaped [3].Osteoclasts secrete collagenase and other enzymes into the subcellular space to make a local acidic environment which dissolves hydroxyapatite and accelerates localized absorption of collagen. Therefore, both cells (osteoblasts, osteoclasts) are coordinated and essential for bone remodeling [4].The bone remodeling process happens with a rate of close to a 100% in the first year of life and 10% in the adult population [5]. The most important micronutrients in maintaining bone health which contribute most to bone mineral density at all ages are calcium, phosphorus, vitamin D [6]. Other studies showed that taking supplements such as calcium and vitamin D promotes bone absorption and resorption [7]. Studies on laboratory animals have also shown that calcium deficiency leads to inhibition of bone formation [8]. Vicky Tai et al., studied the special effects of a diet rich in calcium on bone metabolism in rats. Results indicated that Bone Mineral Density (BMD) of the femur in groups which had consumed calcium rich nutrients were notably higher than that of the control group [9]. During the process of bone formation, fluctuations in estrogen affect bone formation [10].Receptor activator of nuclear factor kappa-B ligand (RANKL), a member of the Tumour Necrosis Factor (TNF) superfamily, is an effective stimulator of both, osteoclast formation and their boneresorbing activity [11]. Upon binding to its receptor, RANK located on osteoclasts, RANKL signaling increases differentiation and activation of the osteoclasts resulting in expression of osteoclast specific molecules. During normal bone remodeling, marrow stromal cells and osteoblasts produce RANKL, which binds to the transmembrane receptor RANK on osteoclast precursors and induces differentiation and activation [12]. This occurs through the transcription factor, nuclear-factor kappa B(NFkB), which is responsible not only for activating osteoclastogenesis but also the body's inflammatory response. Although it has been proposed for a long time that the main source of RANKL are stromal and osteoblastic cells, a very recent study examiners proved that the main RANKL production site resides within osteocytes [13].Osteoprotegerin (OPG) is a secreted by TNF receptor super family member acting as a decoy receptor molecule for RANKL, thereby counteracting its osteoclastogenic activity. It is produced by a variety of cells, including stromal cells, B lymphocytes and dendritic cells [14].Estrogen, the major hormone regulating bone remodeling, is essential for both men and women. Estrogen's role in maintaining bone health is far rea...
The proinflammatory cytokines of TNF-α and IL-1β have been reported to be increased in gastric mucosal surfaces in people with Helicobacter pylori infection. Accordingly, this study was conducted to investigate the relationship between the presence of H. pylori genes and the serum oscillations of these cytokines. In this study, DNA was first extracted from the stool samples of infected individuals and used as DNA template to investigate the presence of glmM and 16S rRNA genes in PCR. The ELISA assay was employed to examine serum levels of TNF-α and IL-1β cytokines. According to statistical analysis, there was a significant correlation between the presence of glmM and 16S rRNA genes in the stool samples of infected persons and the serum oscillations of TNF-α and IL-1β cytokines. At the end of study and analysis of the data in case group with HPSAg+, 47.6% of the glmM gene and 23.6% of the 16S rRNA gene were positive. In addition, a significant correlation was observed between the presence of glmM and 16S rRNA genes in the stool specimens of infected individuals and the serum levels of TNF-α and IL-1β cytokines (p < 0.05). Considering the results, it can be concluded that fluctuations in the amount of HPSA, TNF-α, and IL-1β in H. pylori infection depend on the presence of glmM and 16S rRNA genes. The presence of glmM and 16S rRNA in the stool sample increases by boosting the response level to stool antigen (HPSA), IL-1β, and TNF-α, suggesting the prognosis of the disease with a bacterial virulence form using stool tests.
Introduction:Helicobacter pylori (H. pylori), is a bacterium responsible for upper gastrointestinal tract diseases. The 16s rRNA is a common H. pylori gene which are usually preferred for diagnosis purpose. The aim of this study was to determine the prevalence and abundance of 16s rRNA in fecal samples and also evaluate correlation between the level of 16s rRNA and activities of the cytokines, TNF-α and IL-1β, in serum.
Materials and methods:The present study was performed on 84 subjects with digestion problems. Fecal and blood samples were collected and 16s rRNA gene was assayed using PCR. The serum levels of TNF-α and IL-1β levels were measured by enzyme-linked immunosorbent assay (ELISA).
Results:The results of the study revealed that there was a positive correlation between the 16s rRNA gene, H. pylori stool antigen (HPSA) and TNF-α cytokine. The study also noted that with every unit of increase in either of the quantified parameters of HPSA and IL-1β, the presence of 16s rRNA in fecal samples, showed a 2.98 and 1.01 times rise, respectively. Conclusion: According to the obtained results, it may be concluded that activities of cytokine TNF-a correlated well with the presence of HPSA and 16srRNA gene in the stomach's lining. Increase in the activities of HPSA and TNF-a cytokine could be associated with the presence of 16s rRNA in feces.
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